Obsessive-­compulsive disorder is a neuropsychiatric disorder that often begins in childhood and adolescence and around 40% of cases remains chronically in adulthood. This disorder is very heterogeneous from the phenomenological clinical expression. Due to this heterogeneity, this thesis had as objectives: from the clinical point of view: sociodemographic and clinically characterize a sample of pediatric patients with Obsessive-­‐Compulsive Disorder; from neuroimaging: analyze, by magnetic resonance spectroscopy techniques, differences in concentrations of neurometabolites in the anterior cingulate cortex, as described in the literature area involved in the pathophysiology of OCD, including pediatric patients with OCD and a sample of healthy subjects; from genetics: identify associations between genetic variants of dopaminergic, serotonergic and glutamatergic systems, among others, and the risk of early-­‐onset OCD through a transmission disequilibrium study conducted in families; and finally, study the relationship between the concentrations of these neurometabolites with genetic variants. Our results indicate that patients with OCD in children and adolescents age, have high rates of comorbidity. About 67% of patients in our sample shows a comorbid OCD and 28.6% of them, two or more diagnoses. In terms of neuroimaging, there are significant differences in the concentration of glutamate in patients with early onset OCD related to disease duration (less or more than 24 months) in the anterior cingulate cortex. We also found significantly lower levels of inositol in the region in patients compared to healthy subjects. At the genetic level, HTR1B genetic variants (rs2000292) and GAD2 (rs992990 and rs8190748) are associated with the risk of early-­‐onset OCD. It also seems to be a sexual dimorphism in these associations which would be specific to the HTR1B men and women for GAD2 gene. That is, changes in the serotonergic pathways, glutametergic and GABAergic confer an increased risk of developing OCD early onset and in addition, we found an association between HTR1B, SCL18A1 and GRIA1 polymorphisms and concentrations of neurometabolites in the ACC that it could indicate a key part of biological interaction between the serotonergic and glutamatergic pathways in the pathophysiology of OCD.